Talk:Serotonin releasing agent
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editWiki Education Foundation-supported course assignment
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This article was the subject of a Wiki Education Foundation-supported course assignment, between 3 September 2020 and 14 December 2020. Further details are available on the course page. Student editor(s): Cristiancuev.
Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 09:00, 17 January 2022 (UTC)
Bias in narrative in 'Selectivities and serotonin increases' section
editIt has come to my attention that the section here is biased toward suggesting the main mechanism of fenfluramine is through the 5-HT2C receptor. This narrative is pushed quite heavily by Rothman RB et al. in numerous papers. Fenfluramine does have potent activity when attached to these receptors; however, its binding potential is very low (<1%) compared with endogenous serotonin at 5-HT2C. During rapid exocytotic release of endogenous serotonin (from fenfluramine), synaptic serotonin will be more competitive at 5-HT2C than fenfluramine itself, given its binding potential: binding potential supersedes activity at the receptor. This means that fenfluramine's activity at 5-HT2C is likely dwarfed by the activity of endogenous serotonin (i.e., its main mechanism as an SRA). I suggest this relevant information is inserted to reflect a more impartial account of fenfluramine's mechanism of action.
The relevant citations for what I am saying are mentioned here:
'...however, the binding affinity of fenfluramine for 5-HT2A/B/CR is at most <1% of that of competitive endogenous 5-HT[100],[108],[110]. Indeed, given the high concentration of 5-HT following exocytic release and the finite availability of 5-HT receptors [38],[55],[111],...' within this paper:
Colwell, M. J., Tagomori, H., Shang, F., Cheng, H. I., Wigg, C. E., Browning, M., ... & Harmer, C. J. (2024). Direct serotonin release in humans shapes aversive learning and inhibition. Nature Communications, 15(1), 6617. ScienceContrib992 (talk) 12:34, 9 March 2025 (UTC)